Document Detail


Endothelial cell leptin receptor mutant mice have hyperleptinemia and reduced tissue uptake.
MedLine Citation:
PMID:  23359322     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hyperleptinemia is usually associated with obesity and leptin resistance. Endothelial cell leptin receptor knockout (ELKO) mice without a signaling membrane-bound leptin receptor in endothelia, however, have profound hyperleptinemia without signs of leptin resistance. Leptin mRNA in adipose tissue was unchanged. To test the hypothesis that the ELKO mutation results in delayed degradation and slowed excretion, we determined the kinetics of leptin transfer in groups of ELKO and wildtype mice after intravenous bolus injection of (125) I-leptin and the reference substance (131) I-albumin. The degradation pattern of (125) I-leptin in serum and brain homogenates at different time points between 10 and 60 min was measured by HPLC and acid precipitation. Although ELKO mice had reduced uptake of (125) I-leptin uptake by the brain and several peripheral organs, leptin was more stable in blood and tissue. There was no change in the rate of renal excretion. ELISA showed that serum soluble leptin receptor, known to antagonize leptin transport, had a 400-fold increase, probably contributing to the hyperleptinemia and reduced tissue uptake. Thus, the ELKO mutation unexpectedly increased the stability of leptin but suppressed its tissue uptake. These changes probably contribute to the known partial resistance of the ELKO mice to diet-induced obesity.
Authors:
Hung Hsuchou; Bhavaani Jayaram; Abba J Kastin; Yuping Wang; Suidong Ouyang; Weihong Pan
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  228     ISSN:  1097-4652     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  2013 Jul 
Date Detail:
Created Date:  2013-08-05     Completed Date:  2013-11-13     Revised Date:  2014-08-04    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1610-6     Citation Subset:  IM    
Copyright Information:
Copyright © 2013 Wiley Periodicals, Inc.
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MeSH Terms
Descriptor/Qualifier:
Adipose Tissue / metabolism
Animals
Biological Transport, Active
Brain / metabolism
Endothelial Cells / metabolism
Kidney / metabolism
Leptin / blood*,  metabolism
Mice
Mice, Knockout
Obesity / etiology,  metabolism
Protein Stability
RNA, Messenger / genetics,  metabolism
Receptors, Leptin / deficiency*,  genetics,  metabolism
Serum Albumin / metabolism
Tissue Distribution
Grant Support
ID/Acronym/Agency:
DK54880/DK/NIDDK NIH HHS; DK92245/DK/NIDDK NIH HHS; NS62291/NS/NINDS NIH HHS; R01 DK054880/DK/NIDDK NIH HHS; R01 DK092245/DK/NIDDK NIH HHS; R01 NS062291/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Leptin; 0/RNA, Messenger; 0/Receptors, Leptin; 0/Serum Albumin; 0/leptin receptor, mouse
Comments/Corrections

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